Cardiac hypertrophy is regarded as an adaptive response of the heart to biomechanical, hemodynamic or neurohumoral stimuli, aiming to normalize wall stress and to maintain ventricular function. However, in the long term, cardiac hypertrophy predisposes individuals to heart failure, myocardial infarction and sudden death. We are actively engaged in attempting to understand the cellular and molecular events that underlie the hypertrophic response in the adult heart and the mechanisms involved in the transition to heart failure. Furthermore, we are interested in the study of new therapeutic targets that can induce reversion of cardiac hypertrophy and/or prevent the progression of compensated cardiac hypertrophy to heart failure. Rhythmic and effective cardiac contraction depends on appropriately timed generation and spread of cardiac electrical activity. The basic cellular unit of such activity is the action potential, which is shaped by specialized proteins (channels and transporters) that control the movement of ions across cardiac cell membranes in a highly regulated fashion. Left ventricular hypertrophy and heart failure modify the operation of ion channels and transporters in a way that promotes the occurrence of cardiac rhythm disturbances, a process called arrhythmogenic remodeling. Our Research Group has dilated experience and expertise on cellular cardiac electrophysiological techniques (patch-clamp) to study the cardiac channel remodeling that play an important role in the higher risk for cardiac arrhythmias reported for hypertrophied hearts.